* / † indicates co-first / co-senior authorship.
medRxiv · 2026.07.04.26357214 · 2026
VIDRA models genetic dose-response relationships across common and rare variants to prioritise drug targets, direction of modulation, and biomarkers for thousands of gene-phenotype pairs.
bioRxiv · 2026.02.22.707277 · 2026
Division-resolved single-cell transcriptomics of activated T cells introduces CellDivider, a model that infers proliferative state, and shows immune-disease risk converges on early activation and differentiation rather than proliferative capacity itself.
bioRxiv · 2026.02.10.704860 · 2026
TGlow combines multiplexed imaging and open-source analysis to profile lymphocyte morphology, activation, perturbation responses, and dysfunction at single-cell scale.
bioRxiv · 2025.08.18.670767 · 2025
Pooled iPSC-derived microglia combining eQTL mapping with CRISPR screening link neurodegenerative risk genes, including LRRK2 and TREM2, to phagocytosis and other microglial phenotypes.
Nature Genetics · 54(6): 817–826 · 2022
Single-cell profiling across CD4+ T-cell activation maps dynamic genetic effects on expression and connects immune-disease variants to context-dependent regulation.
Cell Genomics · 2(4): 100117 · 2022
Genetic effects on regulatory T-cell expression and chromatin connect immune-disease loci to Treg mechanisms and candidate therapeutic targets.
Nature Communications · 11: 6283 · 2020
A commentary on how functional follow-up of GWAS variants, from reporter assays to CRISPR screens and single-cell profiling, is accelerating.
Genes & Immunity · 21: 390–408 · 2020
Genomic profiling compares naive and memory T-cell activation and identifies stronger CD28 sensitivity in memory cells, with implications for immune-disease susceptibility.
Frontiers in Genetics · 11: 424 · 2020
A review of the functional genomics approaches used to translate GWAS associations into the cellular mechanisms underlying complex disease.
Nature Genetics · 51(10): 1486–1493 · 2019
Chromatin profiling across stimulated T cells and macrophages identifies the immune-cell states in which disease-associated variants are most active.
